Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

MIG6 Mediates Adaptive and Acquired Resistance to ALK/ROS1 Fusion Kinase Inhibition through EGFR Bypass Signaling.

Molecular cancer therapeutics - 3 Jan 2024

Chen Nan, Tyler Logan C, Le Anh T, Welsh Eric A, Fang Bin, Elliott Andrew, Davies Kurtis D, Danhorn Thomas, Riely Gregory J, Ladanyi Marc, Haura Eric B, Doebele Robert C

Abstract excerpt

Despite the initial benefit from tyrosine kinase inhibitors (TKI) targeting oncogenic ALK and ROS1 gene fusions in non-small cell lung cancer, complete responses are rare and resistance ultimately emerges from residual tumor cells. Although several acquired resistance mechanisms have been reported at the time of disease progression, adaptative resistance mechanisms that contribute to residual diseases before the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Anaplastic Lymphoma Kinase
Share to Biomarkers

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Carcinoma, Non-Small-Cell Lung

Share to Drug Resistance, Neoplasm

Share to ErbB Receptors

Share to Protein Kinase Inhibitors

Share to Protein-Tyrosine Kinases

Share to Proto-Oncogene Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 37748191
DOI: 10.1158/1535-7163.MCT-23-0218
PMCID: PMC10762338

Genes

ALK
ROS1
EGFR
ERRFI1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

MIG6 Mediates Adaptive and Acquired Resistance to ALK/ROS1 Fusion Kinase Inhibition through EGFR Bypass Signaling.PMID 37748191Read ↗

Suppression of Mig-6 overcomes the acquired EGFR-TKI resistance of lung adenocarcinoma.Semantic proximity Read ↗

Suppression of Mig-6 overcomes the acquired EGFR-TKI resistance of lung adenocarcinomaSemantic proximity Read ↗

Mutation of epidermal growth factor receptor is associated with MIG6 expression.Semantic proximity Read ↗

Entrectinib resistance mechanisms in ROS1-rearranged non-small cell lung cancerSemantic proximity Read ↗

Focus on ROS1-Positive Non-Small Cell Lung Cancer (NSCLC): Crizotinib, Resistance Mechanisms and the Newer Generation of Targeted TherapiesSemantic proximity Read ↗

ROS1-ADGRG6: a case report of a novel ROS1 oncogenic fusion variant in lung adenocarcinoma and the response to crizotinibSemantic proximity Read ↗

The induction of MIG6 under hypoxic conditions is critical for dormancy in primary cultured lung cancer cells with activating EGFR mutations.Semantic proximity Read ↗

Acquired MET D1228N Mutations Mediate Crizotinib Resistance in Lung Adenocarcinoma with ROS1 Fusion: A Case Report.Semantic proximity Read ↗

ROS1-rearranged Non-small Cell Lung Cancer.Semantic proximity Read ↗

MAPK Pathway Alterations Correlate with Poor Survival and Drive Resistance to Therapy in Patients with Lung Cancers Driven by ROS1 Fusions.Semantic proximity Read ↗

PF-06463922 is a potent and selective next-generation ROS1/ALK inhibitor capable of blocking crizotinib-resistant ROS1 mutations.Semantic proximity Read ↗

MET gene amplification is a mechanism of resistance to entrectinib in ROS1+ NSCLC.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.